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Biomedical subjects

M Takiguchi

Publications and source records attributed to M Takiguchi.

At least 181 records · Page 10Linked to original sources
PubMed1995

[A case of status asthmatics relieved by long-term inhalation of isoflurane].

A 58 year old man in status asthmatics refractory to drug therapy, was relieved by long-term isoflurane inhalation. In status asthmatics, it takes long time to recover from airway-damage, and inhalation-time will be prolonged in many cases. It is appropriate to use isoflurane because it is devoid of significant adverse effects compared with halothane and enflurane. Especially, isoflurane did not cause an increase in the serum fluoride revel, and will not lead to renal insufficiency in spite of its inhalation for 120 hours. It seems that isoflurane is suitable for long-term inhalation.

Administration, Inhalation↗
PubMed1995

A pilot/introducer needle for central vein cannulation.

A kit for safe and easy insertion of a central vein cannula was devised. A small gauge (22 gauge) metal pilot needle was equipped with a Y-shaped hub which had a side-port to accept a small gauge (0.46 mm) Seldinger guide wire. Once the needle reached the vein, guidewire was threaded in through the side-port. There was no need to remove the pilot needle and no need to repeat vein puncture with a larger-bore needle. Three puncture methods were used with the kit: (1) the central approach via the internal jugular vein, (2) the supraclavicular approach via the junction of the internal jugular vein and subclavian vein, and (3) the infraclavicular approach via the subclavian vein. Each method was used on 20 patients, for total of 60 patients, with a high success rate. Less than 3 minutes were required from puncture to catheter insertion. No serious complications were encountered.

Catheterization, Central Venous↗
PubMed1994

Determination of tissue specificity of the enhancer by combinatorial operation of tissue-enriched transcription factors. Both HNF-4 and C/EBP beta are required for liver-specific activity of the ornithine transcarbamylase enhancer.

The enhancer of the rat ornithine transcarbamylase gene is located 11 kilobases upstream from the transcription start site and has been shown to be hepatoma cell-specific. Using transgenic mice, we showed that this enhancer is capable of activating transcription in a liver-specific manner, inverting the tissue specificity of the homologous promoter that is by itself more active in the small intestine than in the liver. Transient transfection analysis with cultured hepatoma cells indicated that the enhancer activity resides in the approximately 110-base pair region containing four protein-binding sites, two for hepatocyte nuclear factor-4 (HNF-4) and two for CCAAT/enhancer binding protein (C/EBP), both of which are liver-selective transcription factors. Concatemerization of a region containing one HNF-4 and one C/EBP site led to reconstitution of the hepatoma cell-specific enhancer, and intactness of these two sites was strictly required for the enhancer activity. Furthermore, cotransfection experiments showed that both HNF-4 and C/EBP beta are necessary, and neither alone sufficient, for activation of the reconstituted enhancer in nonhepatic cells. Requirement of combinatorial operation of at least two liver-enriched transcription factors for transcriptional activation successfully explains why these liver-selective but not strictly liver-specific factors can confer more restricted liver specificity on transcription of their target genes.

Animals↗
PubMed1994

Identification of the gene encoding a novel HLA-B39 subtype. Two amino acid substitutions on the beta-sheet out of the peptide-binding floor form a novel serological epitope.

Serological analysis suggests the existence of a novel HLA-B39 subtype (HLA-B39N) in the Japanese population. To identify this novel allele, a gene encoding HLA-B39N was cloned and the exons were sequenced. A gene encoding HLA-B39N (B*3904) and B*39011 differs by two nucleotide substitutions at codons 11 and 12 whereas B*3904 and B*39013 differ by three nucleotide substitutions at codons 11, 12, and 312. One nucleotide difference at codon 11 produces a change from serine in B*3901 to alanine in B*3904 whereas another difference at codon 12 changes valine in B*3901 to methionine in B*3904. The residues 11 and 12 are located on the beta-sheet out of the peptide-binding floor and are completely buried in the molecule. These results suggest that the substitutions at these residues alter the conformation of other residues forming epitopes of alloantibodies. Analysis of HLA-B*3901 genes in the Japanese population showed that both B*39011 and B*39013 were observed in the Japanese population. The present study suggests that B*3904 may have evolved from B*39011 rather than B*39013.

Amino Acid Sequence↗
PubMed1994

Effect of single amino acid substitution at residue 167 of HLA-B51 on binding of antibodies and recognition of T cells.

We recently showed that a single amino acid substitution of tryptophane into glycine at residue 167 facing the "A pocket" forms a novel HLA-B51 subtype, B*5103, which is serologically discriminated as HLA-BTA. CDC assay of human alloantisera specific for the HLA-B5 CREG against B*5103- or B*5101-transfected human B-cell line, Hmy2C1R (C1R), supported the belief that human alloantisera can discriminate B*5103 from B*5101 Ag. Moreover, we found that 4D12 anti-B5, B35 CREG mAb cannot bind to B*5103 Ag on C1R cells or L cells although it binds to B*5101 Ag on both cells. These results indicate that alloantibodies can detect a single amino acid substitution at residue 167. Furthermore, it was suggested that 4D12 mAb recognizes the structure formed by the HLA-peptide complex since this mAb did not bind to empty HLA-B5, B35 CREG Ag on RMA-S transfectants. Six of eight anti-HLA-B*5101 CTL clones are not able to kill C1R cells expressing B*5103, indicating that conformational change of the A pocket by substitution at residue 167 has a crucial influence on recognition of alloreactive T cells. Therefore, discrimination of B*5103 from B*5101 would seem to be important in bone marrow transplantation.

Amino Acid Sequence↗
PubMed1994

Normalization of hair growth in sparse fur-abnormal skin and hair (SPF-ASH) mice by introduction of the rat ornithine transcarbamylase (OTC) gene.

The sparse fur-abnormal skin and hair (SPF-ASH) mouse is a model for the human X-linked hereditary disease, ornithine transcarbamylase (OTC) deficiency. This condition is characterized by abnormal skin and delayed hair growth, hyperammonemia, orotic aciduria and low levels of serum citrulline and arginine. Murakami et al. [1] established a line of transgenic mice, by introducing the recombinant rat OTC (rOTC) gene into fertilized C57BL mouse eggs. We introduced the rOTC gene into SPF-ASH mice by mating SPF-ASH heterozygotes and transgenic mice, which carried this gene. The hemizygous SPF-ASH mice bearing the rOTC gene showed normal hair growth without sparse fur, normal urinary orotic acid excretion and normal serum citrulline and arginine levels. These mice showed OTC activities 2 and 6 times higher in the liver and small intestine, respectively, than the SPF-ASH mice but about 12% and 27% those of the controls [2].

Animals↗
PubMed1994

HLA-B*3501-peptide interactions: role of anchor residues of peptides in their binding to HLA-B*3501 molecules.

Two HLA-B*3501 binding self-peptides, LPFDFTPGY (37F) and LPGPKFLQY (28H), were isolated from HLA-B*3501 molecules expressed by cultured human B lymphoid cells. Both sequences were consistent with previously reported motifs of HLA-B*3501 binding peptides which carry proline at position 2 and tyrosine at position 9 as anchor residues. Direct binding of these peptides to HLA-B*3501 molecules was quantitated by flow cytometry analysis of RMA-S cells. transfected with the HLA-B*3501 gene (RMA-S-B*3501). Both 37F and 28H peptides bound effectively to HLA-B*3501 molecules. Substitution of amino acids at position 2 and/or 9 of HLA-B*3501 binding peptides markedly reduced their binding to HLA-B*3501 molecules. These results indicate that two anchor residues, proline at position 2 and tyrosine at position 9 are critical in binding of peptides to HLA-B*3501 molecules. Insertion of up to four glycine residues at position 8 of the peptide 37F did not affect its binding affinity to HLA*3501 molecules. These results indicate that long peptides can effectively bind to HLA class I molecules provided that anchor residues are conserved.

Amino Acid Sequence↗
PubMed1994

The role of the conserved residue in pocket A and the polymorphic residue in pocket E of HLA-B*3501 in presentation of human minor histocompatibility peptides to T cells.

We investigated T cell recognition for human minor histocompatibility (hmH) peptides using HLA-B*3501 restricted, hmH specific cytotoxic T lymphocytes (CTL) clones. These CTL clones killed C1R cells expressing HLA-B*3501 but not C1R cells expressing chimeric antigens between HLA-B*3501 and HLA-B*5101. They also failed to kill C1R cells expressing HLA-B*3501 mutants at residue 152 (B*3501-V152E) or at residue 171 (B*3501-Y171H). The CTL clone failed to kill C1R cells expressing these mutant molecules loaded with the hmH peptides isolated from C1R-B*3501 cells although it killed a self-B cell line expressing HLA-B3501 loaded with the specific hmH peptides. The CTL clone also failed to kill T2 cells expressing the mutant molecules loaded with the specific peptides whereas it killed T2 cells expressing HLA-B*3501 loaded with the specific peptide. On the other hand, naturally occurring specific hmH peptides were isolated from purified B*3501-V152E and B*3501-Y171H molecules, indicating that both HLA-B*3501-V152E and HLA-B*3501-Y171H molecules can bind the hmH peptides. These findings indicate that both the conserved residue 171 in pocket A and the polymorphic residue 152 in pocket E are critical in recognition of the T cells but not binding of the hmH peptides. Furthermore, these results provide the possibility that the TCR recognizes a conformational structure of hmH peptides bound to HLA-B*3501 molecules.

Antigen Presentation↗
PubMed1994

The delayed glucocorticoid-responsive and hepatoma cell-selective enhancer of the rat arginase gene is located around intron 7.

Liver-selective transcription of the gene for rat arginase, an ornithine cycle (urea cycle) enzyme, is induced by glucocorticoids in a delayed secondary manner; the mRNA induction by the hormones requires de novo protein synthesis, and is preceded by a time lag of several hours. We searched for a DNA element mediating the glucocorticoid induction of the arginase gene with a transient transfection system using hepatoma cell lines. Within the 233-base pair region that is located 11 kilobases downstream from the transcription start site and that spans the junction of intron 7 and exon 8, we detected an enhancer element that is glucocorticoid-responsive and hepatoma cell-selective. The time course of the glucocorticoid induction through this enhancer element was delayed compared to that through the primary glucocorticoid-responsive mouse mammary tumor virus promoter. Footprint analysis revealed four protein-binding sites in this enhancer region. In gel retardation analysis, each site exhibited a complicated profile characterized by a number of shifted bands, some of which were tissue-selective and others ubiquitous. Gel shift competition and antibody supershift/inhibition analysis demonstrated that two of the four sites are recognized by members of the CCAAT/enhancer binding protein (C/EBP) family, some of which are liver-enriched.

Animals↗
PubMed1994

Rat argininosuccinate lyase promoter: the dyad-symmetric CCAAT box sequence CCAATTGG in the promoter is recognized by NF-Y.

The gene for rat argininosuccinate lyase (AL), which catalyzes the last step of arginine biosynthesis, is expressed in many tissues, though its expression is much higher in the liver where the enzyme is involved in the ornithine cycle (urea cycle), and moderately higher in the kidney. In transient transfection analysis using various cell lines, the AL promoter exhibited considerable levels of activity in all tested cell lines, with no apparent liver cell specificity, presumably reflecting the ubiquitous expression of this gene. Analysis of 5'-deletion mutants of the promoter region revealed several cis-regulatory elements, whose contribution to the promoter activity seemed to vary according to cell type. The most prominent positive regulatory region was detected around the position -80 base pairs, and it overlapped with a dyad-symmetric CCAAT box sequence CCAATTGG. A factor(s) interacting with this sequence element was found to be present ubiquitously. Gel shift competition analysis and antibody double shift analysis showed that this factor was identical or highly similar to a transcription factor, nuclear factor-Y (NF-Y), which consists of two different subunits and recognizes CCAAT motifs in various promoters. Point mutagenesis at each half site of the palindrome CCAATTGG and the introduction of a space between the half-site motifs abolished the binding with NF-Y. Thus, it seems that NF-Y recognizes the correctly spaced dyad-symmetric CCAAT box.

Animals↗
PubMed1994

Evaluation of dynamic response of catheter-manometer systems for pulmonary arterial pressure.

To quantitatively evaluate the waveform distortions observed through a catheter-manometer system, the tolerance range of amplitude errors and that of phase errors are defined as both within +/- 5%, and the frequency bandwidth was calculated where the frequency characteristics of amplitude and those of phase difference satisfy the two tolerance ranges by use of a second-order kinetic equation. The results were expressed by three variables, composed of the natural frequency (fn), damping coefficient (zeta), and highest frequency (fh) corresponding to the frequency bandwidth; a chart was constructed with fn on the x-axis, zeta on the y-axis, and fh as parameter. Also on the chart, the propagation delay times (td's) determined by fn, zeta, and fh were plotted. We measured the frequency characteristics of two 7-Fr Swan-Ganz catheters with lengths of 75 and 110 cm. fn's and zeta's were found to be 13.9 and 10.1 Hz and 0.23 and 0.32, respectively. Referring to this chart, the maximal fh these catheters would be able to reproduce within the tolerance ranges and the propagation td's can be predicted to be 3.2 and 2.4 Hz and 7 and 12 ms, respectively. Suppression of resonance by use of Accudynamic improved the maximal fh's to 3.9 and 2.9 Hz, respectively, but resulted in the increased td's to 14 and 19 ms due to increased zeta.

Blood Pressure Determination↗
PubMed1994

Scintigraphic and ultrasonographic diagnosis of soft tissue injury in a thoroughbred horse.

A 2.5-year-old female Thoroughbred horse was referred to the veterinary teaching hospital for right front limb lameness of 1 year duration. Physical examination and diagnostic nerve blocks failed to localize the origin of the lameness. Scintigraphy with 99mTc-MDP suggested increased radionuclide uptake in the palmar metacarpal soft tissues of the right front limb. Ultrasonographic examination revealed hypoechoic lesions in the superficial digital flexor tendon and the suspensory ligament, suggesting tendinitis and desmitis. Combined imaging modalities improved detection and characterization of the cause of a long-standing obscure lameness.

Animals↗
PubMed1994

Potentiation of neuromuscular blockade by calcium channel blockers.

A significant reduction was noticed in the amount of vecuronium needed to maintain steady neuromuscular blockade at 20% twitch height (T1) in patients given nicardipine intraoperatively. Bolus injection of either nicardipine or diltiazem during constant infusion of vecuronium produced transient depression of T1 and the train-of-four ratio (TOFR). Reversal of neuromuscular blockade with a choline esterase inhibitor (neo-stigmine) was not retarded by previous administration of Ca-channel blockers but concurrent administration of anticholine-esterase agent and Ca-channel blockers caused a delay in recovery from motor blockade. Monitoring of neuromuscular junction activity is strongly recommended whenever a large cumulative dose of Ca-channel blockers is used.

Adult↗